Folic Acid Awareness Week 2015: Want Awareness? Here You Go

Optimizing the health of unborn children is my passion.

I am pleased to state that January is named National Birth Defects Prevention Month by the National Birth Defects Prevention Network and the CDC. This month is broken down into four parts with each part focusing on a key component of birth defect prevention.

While I should be completely supportive of this fantastic cause, I am not. In fact, I am totally and utterly against one of their causes blended in with reducing birth defects.

Why?

Because it has to do with folic acid. My arch enemy. And it is also the arch enemy of unborn children – and children in general.

Folic Acid Awareness Week extends from January 5 – 11. Happily, I am extending the Folic Acid Awareness cause for years to come – only my cause is to establish folic acid as an anti-nutrient which is causing significant harm.

Yes, there are countless research papers out there which show that folic acid reduces neural tube defects. This is true. According to the Harvard Medical School:

In countries that require folic acid fortification, including the United States and Canada, the rate of neural tube defects has fallen by 25% to 50%. 

After all, folic acid has no use biochemically in the body until it is converted into these other forms of folate such as:

• Tetrahydrofolate (THF)
• 5-formyltetrahydrofolate (Folinic acid)
• 5-10-methylenetetrahydrofolate
• 5-methyltetrahydrofolate (Methylfolate)

Let’s view how folic acid is changed into usable forms of folate by the body:

That appears to be a lot of work right?

It is.

And this is a very simplified outline of what it takes to convert folic acid into usable forms.

Imagine a mother – or child – or father – who has a problem in any one of these genes.

Then add on a potential deficiency of vitamin B12 (which is fairly common and often goes undiagnosed for years).

What happens is far from good.

You see the ‘Folic Acid’ moving to ‘DHF’ in the diagram above? Note how it states this is a ‘slow’ process?

Now note the dashed black arrow moving from ‘Folic Acid’ to ‘UMFA’

What is ‘UMFA’?

UMFA is the sound your body makes when you ingest too much folic acid. ‘Ummph’ It hurts.

Truly? UMFA = unmetabolized folic acid

What does that mean?

It means folic acid didn’t get processed by the body into usable forms of folate so your blood just has this synthetic nutrient floating around in it.

Is that ok?

According to researchers Obeid and Hermann:

Evidence of a negative health effect of free folic acid (FA) in blood is not consistent and suggests rather artificial factors. FA has no known cofactor function that would increase the likelihood of a causal role for free FA in disease development.

This means that since folic acid is totally synthetic, it doesn’t do anything to the body’s enzymes thereby rendering it harmless.

Let’s look at a compound which is a known killer: Carbon Monoxide.

How does carbon monoxide kill? Carbon monoxide kills because it preferentially binds to your hemoglobin 210 times stronger than oxygen which means your hemoglobin cannot bind oxygen well in the presence of carbon monoxide. The higher the levels of carbon monoxide, the less oxygen is bound to your hemoglobin causing decreased oxygenation and cell death.

Does folic acid do the same thing?

Yes, if you examine how folic acid binds to folate binding proteins (these carry folate around your body, the developing baby and breast milk) and folate receptors (these pull folate inside the cell and out of the blood) in the human body. Folic acid binds preferentially to folate binding proteins and folate receptors. This means that the folate binding proteins and folate receptors in your body, which are intended to bind methylfolate or folinic acid, are more likely to bind to synthetic folic acid.

The Annual Review of Nutrition published an article in 1990 states, “A major class, the high-affinity folate-binding proteins, show a preferential and tight binding of folic acid relative to reduced folates . . . Soluble forms of the high-affinity binders are present in serum and [breast]milk. [Folate binding proteins] serve to accumulate and stabilize reduced-folate compounds in milk and they may also facilitate the absorption of folates by the intestinal mucosa of neonates.”

If high-affinity folate binding proteins are bound to synthetic and inactive folic acid, what benefit is there to the developing baby? In fact, it would make sense that harm would occur as reduced folates are needed for DNA production, balance methylation and support neurological development.

How can reduced folates get into the intestinal mucosa of the baby if they are not bound to the folate binding proteins? Are we setting up our new generation with weakened intestinal linings? Food allergies are definitely on the rise.

Autism is definitely on the rise and we all know those with autism have significant gut issues.

We know that synthetic folic acid reduces the incidence of neural tube defects. What about if we used methylfolate instead? Can methylfolate reduce the incidence of neural tube defects?

Individuals show wide variations in their ability to reduce folic acid (FA). Carriers of certain polymorphisms in genes related to folate metabolism or absorption can better benefit from 5-methylTHF instead of FA. 5-MethylTHF [also known as (6S)-5-methylTHF] is the predominant natural form that is readily available for transport and metabolism. In contrast to FA, 5-methylTHF has no tolerable upper intake level and does not mask vitamin B12 deficiency. Supplementation of the natural form, 5-methylTHF, is a better alternative to supplementation of FA, especially in countries not applying a fortification program. Supplemental 5-methylTHF can effectively improve folate biomarkers in young women in early pregnancy in order to prevent NTDs.

For a moment, let’s move away from how folic acid in utero and see how folic acid affects breast milk.

When looking at how breast milk is affected by synthetic folic acid, one cringes.

“…recent evidence suggests that the somewhat higher affinity of folate binding protein for folic acid than for reduced forms may also decrease the bioavailability of milk folate. . . The markedly lower concentration of milk folate binding proteins compared with prefortification reports along with detectable appearance of unmetabolized folic acid in the milk of even unsupplemented mothers emphasizes the ongoing need to evaluate the potential benefits and risks of long-term consumption of folic acid-fortified foods.”

This means that synthetic folic acid reduces the production of folate binding protein. If folate binding proteins are reduced, then the reduced folates are not getting delivered to the breast fed baby. If the baby is not getting adequate reduced folates, then their methylation and DNA production is negatively affected.

Again, autism is on the rise and so are food allergies – not to mention other neurological disorders and mental/emotional issues. Tough to have a healthy baby with decreased amounts of beneficial folate in their body.

Let’s look at a paper which evaluates how effective folic acid is compared to methylfolate at increasing plasma folate levels. After all, we are looking to increase plasma folate levels in order to reduce birth defects right? There is a plethora of research which associates higher plasma folate levels to decreased rates of birth defects. So let’s look at these two side by side.

The British Journal of Pharmacology published a paper in 2009 entitled, “[6S]-5-methyltetrahydrofolate increases plasma folate more effectively than folic acid in women with the homozygous or wild-type 677C–>T polymorphism of methylenetetrahydrofolate reductase.”

Need I say more?

I’m going to – and I need to.

Note that the researchers only measured ‘plasma folate’. They did not measure intracellular folate. This is important. Can you think of why? Remember that synthetic folic acid binds to folate binding proteins and folate receptors on the cell preferentially over reduced folates like folinic acid and methylfolate?

If this is the case, then we should actually see a decrease in intracellular folate levels in the presence of synthetic folic acid, right?

We do.

That’s bad.

Doctors every day are tricked into thinking their patient’s homocysteine levels are reducing. But what are they checking? They are only checking the blood levels of homocysteine – not intracellular levels nor are they measuring methylation status.

If we want to reduce the incidence of birth defects and optimize the health of unborn children, we need to support one carbon metabolism (aka methylation) in future parents prior to pregnancy. In fact, we really shouldn’t be limiting our attention to folate levels at all – we need to be focused on the bigger picture of what folate actually does – and that is regulate methylation.

Finnell et al say it best: “The effect of one-carbon metabolism on normal neural tube closure extends far beyond just folic acid.”

Then they throw down the gauntlet:

During early embyrogenesis, DNA methylation, which is the chief regulator of gene expression, is epigenetically programmed. Furthermore, it has been well established that methylation of DNA can be influenced by dietary contributions of methyl donors such as choline, folate, and methionine. Any suboptimal methyl-donor supply could alter DNA methylation and provide a ready explanation for a possible mechanism contributing to increase birth defect risk.

Finnell et al. published this in 2010.

It is now 2015.

With the information era exploding with countless ways to access research like this, why aren’t groups like National Birth Defects Prevention Network and the CDC accessing it? I mean, aren’t they wanting to reduce birth defects?

Things evolve.

Folic acid is old hat, out-dated, worn out and needs to go away. And now.

National associations and physicians need to engage, access current research, digest it and implement it.

How did folic acid get into the foods anyhow if it is so bad?

Great question.

Rats and mice are used in research as their genetics and gene function are very similar to ours – as humans. However, there are variations at times.

Folic acid metabolism is one HUGE variation.

You see, in the mouse, their folic acid reducing enzyme, the first one, called dihydrofolate reductase (DHFR) is very adept at reducing folic acid into dihydrofolate.

In humans, we do not have a fast DHFR enzyme and so the folic acid bogs our biochemistry down significantly. As it sits around and waits to get reduced into active folates, it ends up binding to folate binding proteins and folate receptors which prevent active folates from doing so – as described above.

Even mice are negatively affected from folic acid!

A very recent study JUST published came out for this lovely Folic Acid Awareness Week – thank you!

Key findings from this paper state that high dose folic acid, 10x higher than recommended, contributes to MTHFR deficiency and thus liver issues.

Why liver issues?

Because the liver does about 85% of all methylation reactions so it is one of the first organs to get negatively affected.

“We suggest that high folic acid consumption reduces MTHFR protein and activity levels, creating a pseudo-MTHFR deficiency.
This deficiency results in hepatocyte degeneration, suggesting a 2-hit mechanism whereby mutant hepatocytes cannot accommodatethe lipid disturbances and altered membrane integrity arising from changes in phospholipid/lipid metabolism. These preliminary findings may have clinical implications for individuals consuming high dose folic acid supplements, particularly those who are MTHFR deficient.”

Ouch.

Look at all the foods, drinks and supplements which have folic acid in them. Then add up how much folic acid you think you consume in a day. Yes, some people are deficient, but there are also many that are getting way too much.

Folic acid is not what we should be recommending anyway. We should be recommending folinic acid and methylfolate. The days of folic acid should be numbered. It’s an old, archaic ingredient that needs to be tossed. Nutritional biochemistry has evolved significantly. There is no reason to keep using folic acid at all. The only reason to keep using it is because it is inexpensive and companies which use it are making more money off it is due to higher gross margins. Folinic acid is not that expensive. Methylfolate, however, is extremely expensive.

Lab Testing Your Folate Levels: UMFA, Methylfolate and Others

UPDATE: Jan 2015, the UMFA test is no longer available as doctors did not order it enough so the lab discontinued it. This goes to show you that awareness is still very low about the harms of folic acid and UMFA levels.

Some laboratory testing companies are cutting edge and offering UMFA lab testing along with reduced folate testing. Genova is one lab and another is Health Diagnostics. Your doctor can open an account with one or both of these labs and begin identifying your folate levels properly. If you don’t have a doctor or they cannot order it for you for various reasons, you may order the UMFA Test here and the Methylation Profile Test

Here is what the UMFA Lab Result looks like. Note that they show both UMFA and Methylfolate levels.

What to do? Action Steps

1. Throw out all folic acid enriched foods. These are processed foods such as cereals, breads, pastas, energy bars, drinks, snacks.
2. Throw out all folic acid containing supplements.
3. Eat folate rich foods. Note that when I state folate, I mean naturally-occurring folates such as dihydrofolate, folinic acid and methylfolate.
   • uncooked leafy greens (more you cook greens, the more folate gets destroyed)
   • beef liver (organic, free range)
   • various beans such as lentils, pinto, garbanzo, black, navy, kidney and lima.
4. Opt for supplements containing active folates. Many quality supplement companies are moving in this direction. Seeking Health is the supplement company I created in order to provide physicians and the general public researched ingredients and effective formulations.
5. Test your methylation pathway with your physician and see which forms of folate you are low or high in – then correct it.
6. Test your genetics and see where you may have blocks in your folate pathway. Knowing this is useful as you can be proactive in bypassing these blocks with various nutrients, avoiding various medications and increasing certain foods.
7. After you test your genetics via 23andMe, then run your raw data through StrateGene.

I encourage you, as an individual looking to optimize your health and possibly your future child’s, to inform your physician, friends and loved ones about the dangers of folic acid – and the benefits of reduced folate such as methylfolate.

Health professional or just want to understand the significance of methylation dysfunction during pregnancy, childhood and adulthood?

Two online courses are now available to learn in DETAIL about the harms of folic acid and in depth education about the importance of methylation – how it is affected and how to restore it.

Maternal and Pediatric Implications due to MTHFR and Methylation Dysfunction – this is an absolute must for pediatricians, OB/GYN, midwives, doulas, nutritionists and those wanting to have children.

Methylation and Clinical Nutrigenomics: Part 1

For those who desire more information but not as in depth as the two courses above, I highly recommend this free video discussing folate metabolism:

Folate Metabolism

I believe that it is possible to reduce the incidence of disease of unborn children – and I will do this one physician and one person at a time.

There is nothing more powerful in preventative medicine than reducing disease in the unborn child.

Thank you

Dr Lynch

PS – Throw away your folic acid enriched foods and supplements. Today. That is your way to celebrate Folic Acid Awareness Week 2014. Spread the word.

PPS – Read how folic acid fortification may be associated with increased rates of autism.

PPPS – Learn about prenatal supplementation

by Dr. Ben Lynch on January 8, 2014 in Rants & Raves